心脏受损后几乎没有再生能力，所以了解产生新的心肌细胞所需因素是人们非常感兴趣的问题。
Jun Takeuchi 和Benoit Bruneau对小鼠中胚层向心肌细胞的分化转移进行了研究，发现两个心肌转录因子和BAF染色质重塑复合物的一个心肌特异性亚单元足以引导小鼠中胚层向扩张的心肌细胞的转化。再增添一个转录因子，会促进向收缩的心肌细胞的转化，促进对非心肌中胚层基因的抑制。确定心肌细胞分化的要求，从长远来讲可帮助实现再生用于治疗的心肌细胞的目标。(生物谷Bioon.com)
生物谷推荐原始出处：
Nature 459, 708-711 (4 June 2009) | doi:10.1038/nature08039
Directed transdifferentiation of mouse mesoderm to heart tissue by defined factors
Jun K. Takeuchi1,2 & Benoit G. Bruneau1,3
1 Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA
2 Division of Cardiovascular Research, Global-Edge Institute, Tokyo Institute of Technology, Frontier S2-16, Nagatsuda, Midori-ku, Yokohama, Kanagawa 226-8503, Japan
3 Department of Pediatrics, Cardiovascular Research Institute, and Institute for Regeneration Medicine, University of California, San Francisco, California 94158, USA
Heart disease is the leading cause of mortality and morbidity in the western world. The heart has little regenerative capacity after damage, leading to much interest in understanding the factors required to produce new cardiac myocytes. Despite a robust understanding of the molecular networks regulating cardiac differentiation1, 2, no single transcription factor or combination of factors has been shown to activate the cardiac gene program de novo in mammalian cells or tissues. Here we define the minimal requirements for transdifferentiation of mouse mesoderm to cardiac myocytes. We show that two cardiac transcription factors, Gata4 and Tbx5, and a cardiac-specific subunit of BAF chromatin-remodelling complexes, Baf60c (also called Smarcd3), can direct ectopic differentiation of mouse mesoderm into beating cardiomyocytes, including the normally non-cardiogenic posterior mesoderm and the extraembryonic mesoderm of the amnion. Gata4 with Baf60c initiated ectopic cardiac gene expression. Addition of Tbx5 allowed differentiation into contracting cardiomyocytes and repression of non-cardiac mesodermal genes. Baf60c was essential for the ectopic cardiogenic activity of Gata4 and Tbx5, partly by permitting binding of Gata4 to cardiac genes, indicating a novel instructive role for BAF complexes in tissue-specific regulation. The combined function of these factors establishes a robust mechanism for controlling cellular differentiation, and may allow reprogramming of new cardiomyocytes for regenerative purposes.
